Humans ; Critical Illness ; Multiple Organ Failure/etiology*

Burns ; complications ; Humans ; Multiple Organ Failure ; etiology ; prevention & control

The prevention and treatment of complications are very important aspects in burn treatment. We should pay attention to the fundamental research, clinical prevention and treatment of complications. We have had good grasp of the subjects by fundamental research such as MODS. We must keep complications in mind when signs, symptoms, monitoring index and laboratory reports are inconsistent to the usual course of the injury, and we must guard against the occurrence of complications in the whole course of burn treatment. Consideration must be given to the treatment of both complications and the primary disease in order to slow down deterioration of patient, and guarantee the curative effect. There are still many unknown areas of burn complications for us to explore and discover.
Burns ; complications ; Multiple Organ Failure ; etiology ; prevention & control

Most of the major advances in the prevention and treatment of burn sepsis and MODS have been made within the last 20 years. Improvements have been made in gaining a better understanding of the pathophysiology of burn sepsis and MODS, in revising the definition of sepsis and MODS, and in prevention and treatment of burn shock. Additionally, improvements have been made in fluid resuscitation in patients with burn shock and in early gastrointestinal feeding to prevent translocation of endotoxins from the gut. Other achievements have been made in using recombinant human growth hormone combined with intensive insulin therapy to control hyperglycemia, and potassium chloride to prevent hypokalemia in order to accelerate protein synthesis. Additional advances include early closure and coverage of the burn wound, rational use of antibiotics, immunological modulation to combat immunological dissonance. Also, advances have been made by using early anticoagulation treatment to prevent coagulopathy. In prevention and treatment of burn sepsis and MODS, comprehensive support for all organs during the course of treatment is emphasized. Although the advances in burn treatment have been extremely encouraging over the last 50 years, burn sepsis and MODS remain the most common cause of mortality in the critical ill. To cope with extreme environmental conditions, such as armed conflict and natural disasters, research is needed to optimize the oral resuscitation regime, and more efficacious treatment strategies that are based on an indepth understanding of the pathogenesis of sepsis.
Burns ; complications ; metabolism ; Humans ; Multiple Organ Failure ; etiology ; prevention & control ; Sepsis ; etiology ; prevention & control

Burns ; complications ; metabolism ; Endotoxemia ; etiology ; metabolism ; Humans ; Multiple Organ Failure ; etiology ; metabolism ; Myocytes, Cardiac ; metabolism

Multiple organ dysfunction (or failure) syndrome (MODS or MOFS) remains a hurdle for us to overcome before further improvement in the survival rate can be achieved in the patients with extensive deep burns. It is, however, generally recognized that MODS is the final result of the liberation and interplay of multiple inflammatory mediators or cytokines, and there is a two hit phenomenon in its pathogenesis. In extensive burns, the first hit is usually the burn injury itself and the ensuing hypovolemic shock, followed by septic response. The large amount of devitalized tissues, along with the development of invasive infection, constitutes frequently the second hit. Since as yet nearly all therapeutic strategies directed specifically toward neutralizing inflammatory mediators or cytokines to control sepsis have failed in clinical trials, and the treatment of established organ failure is usually not successful, it is deemed rational to focus our attention instead on the prevention of this dreadful syndrome in the clinical practice. It is our belief that the strategies of treatment should be: blunt the first hit and prevent the second hit and supplemented with visceral support and nutritional support.
Burns ; complications ; Cytokines ; adverse effects ; Endotoxemia ; etiology ; Humans ; Hypovolemia ; etiology ; Multiple Organ Failure ; etiology ; prevention & control ; Sepsis ; etiology ; Shock ; etiology

Presented in this paper is our experience in the diagnosis and management of abdominal compartment syndrome during severe acute pancreatitis. On the basis of the history of severe acute pancreatitis, after effective fluid resuscitation, if patients developed renal, pulmonary and cardiac insufficiency after abdominal expansion and abdominal wall tension, ACS should be considered. Cystometry could be performed to confirm the diagnosis. Emergency decompressive celiotomy and temporary abdominal closure with a 3 liter sterile plastic bag must be performed. It is also critical to prevent reperfusion syndrome. In 23 cases of ACS, 18 cases received emergency decompressive celiotomy and 5 cases did not. In the former, 3 patients died (16.7%) while in the later, 4 (80%) died. Total mortality rate was 33.3% (7/21). In 7 death cases, 4 patients developed acute obstructive suppurative cholangitis (AOSC). All the patients who received emergency decompressive celiotomy 5 h after confirmation of ACS survived. The definitive abdominal closure took place mostly 3 to 5 days after emergency decompressive celiotomy, with longest time being 8 days. 6 cases of ACS at infection stage were all attributed to infected necrosis in abdominal cavity and retroperitoneum. ACS could occur in SIRS stage and infection stage during SAP, and has different pathophysiological basis. Early diagnosis, emergency decompressive celiotomy and temporary abdominal closure with a 3L sterile plastic bag are the keys to the management of the condition.
*Abdomen ; *Compartment Syndromes/diagnosis ; *Compartment Syndromes/etiology ; *Compartment Syndromes/surgery ; Decompression, Surgical ; *Multiple Organ Failure/diagnosis ; *Multiple Organ Failure/etiology ; *Multiple Organ Failure/surgery ; *Pancreatitis, Acute Necrotizing/complications ; *Pancreatitis, Acute Necrotizing/diagnosis ; *Pancreatitis, Acute Necrotizing/surgery

Heat stroke is a potentially fatal disorder that's caused by an extreme elevation in body temperature. We report here an unusual case of multiple organ failure that was caused by classical, nonexertional heat stroke due to taking a warm bath at home. A 68 year old diabetic man was hospitalized for loss of consciousness. He was presumed to have been in a warm bath for 3 hrs and his body temperature was 41 degrees C. Despite cooling and supportive care, he developed acute renal failure, disseminated intravascular coagulation (DIC) and fulminant liver failure. Continuous venovenous hemofiltration was started on day 3 because of the progressive oligouria and severe metabolic acidosis. On day 15, septic ascites was developed and Acinetobacter baumanii and Enterococcus faecium were isolated on the blood cultures. In spite of the best supportive care, the hepatic failure and DIC combined with septic peritonitis progressed; the patient succumbed on day 25.
Multiple Organ Failure/*etiology ; Male ; Liver Failure/*etiology ; Kidney Failure/*etiology ; Humans ; Heat Stroke/*complications/etiology ; Fatal Outcome ; Baths/*adverse effects ; Aged

OBJECTIVETo study the reliability of establishing a neonatal piglet model of multiple organ dysfunction syndrome (MODS) by cecal ligation and puncture (CLP).

METHODSFourteen neonatal piglets were randomly assigned into Experiment group (n=9) and Control group (n=5). MODS model was established in the piglets from the Experiment group by CLP. The Control group underwent a sham-operation. Serum biochemical parameters (ALT, AST, ALB, BUN, Cr, CK-MB and lactic acid), blood platelet counting and blood gas analysis(PaO2 and PaCO2) were tested at 0, 24, 48, 72, 96, and 120 hrs after operation. The histomorphological changes of important vital organs were examined by hematoxylin-eosin staining under a light microscope.

RESULTSThe levels of serum ALT, AST, BUN, Cr, CK-MB and lactic acid in the Experiment group began to increase 24 hrs after operation. Significant differences were observed between the Experiment and the Control group at 48 hrs in ALT (83.0 +/- 9.3 U/L vs 57.8 +/- 15.8 U/L), AST (348.8 +/- 132.9 U/L vs 106.4 +/- 12.5 U/L), BUN (10.5 +/- 2.5 micromol/L vs 4.3 +/- 1.0 micromol/L), Cr (79.2 +/- 9.0 micromol/L vs 53.6 +/- 6.8 micromol/L), CK-MB (5152.0 +/- 1 857.8 U/L vs 1243.0 +/- 354.5 U/L), and lactic acid (12.3 +/- 4.0 mmol/L vs 4.6 +/- 1.5 mmol/L) (P < 0.01). The high levels of the above parameters persisted until 96 hrs after operation in the Experiment group and then decreased but were still higher than those at 0 h after operation. After operation, the blood platelet counting decreased significantly at 96 hrs, and PaO2 decrease and PaCO2 increase were observed at 48 hrs in the Experiment group compared with the Control group. All animals, except one, in the Experiment group died within 120 hrs after operation (with the MODS incidence of 56%), while none died in the Control group. The tissue injuries with different degrees were observed in the lungs, liver, heart, kidneys and gastrointestinal tracts of the Experiment group.

CONCLUSIONSNeonatal piglet MODS model can be established successfully by CLP.

Animals ; Animals, Newborn ; Disease Models, Animal ; Female ; Male ; Multiple Organ Failure ; blood ; etiology ; pathology ; Swine

Adult ; Humans ; Male ; Multiple Organ Failure ; etiology ; Thyroid Crisis ; complications ; Wounds and Injuries ; complications